The mortality associated with SARS and pandemic influenza is linked to rapidly progressive respiratory failure causing acute lung injury (ALI) or acute respiratory distress syndrome (ARDS). In some cases, multi-organ failure is also a feature. In the case of pandemic H5N1 influenza, the mortality due to respiratory and multi-organ failure is around 60%. The primary lung pathology of fatal H1N1 influenza has recently been described and is characterised by necrotising alveolitis and dense neutrophil infiltration [1].
Originally, it was assumed that respiratory failure associated with SARS and pandemic influenza was due to rapid viral replication leading to cytolytic destruction of target cells of the respiratory tract, such as alveolar epithelial cells, or to escape of the virus to tissues and organs remote from the respiratory system, such as the central nervous system. Recent evidence has shown, however, that the development of respiratory failure is not, in fact, associated with high viral titres. Investigators have instead found that respiratory failure is associated with significant elevation of pro-inflammatory cytokines such as TFNa and IFNβ. This has led experts to propose that the pathogenesis of these complications is inappropriate stimulation of the innate immune system triggering a so-called ‘cytokine storm’ [2, 3].
Current treatments for respiratory failure involve increasing the patient's oxygen levels using an oxygen mask, mechanical oxygenation using a ventilator or, in the most severe case, extracorporeal membrane oxygenation (ECMO) which involves circulating the patient's blood outside the body and adding oxygen to it artificially
There is a great need for agents that improve upon the currently available treatments for the respiratory failure caused by the inflammatory effects of viral infection of the respiratory tract.